Abstract
Background: Organic “nitro” compounds such as nitroglycerine, isosorbide dinitrate are useful in the control of chest pain in acute coronary syndrome. But the mechanism of it in pain regulation remains speculative. Here, increase of NO production was investigated by the possible regulation of constitutive nitric oxide synthase (cNOS) function from goat arterial endothelial cells. This protein was purified and sequence wise characterized as protein disulfide isomerase (PDI) in response to different nitro compounds.
Method: The NO generating protein was isolated from arterial endothelial cells and prepared to homogeneity. NO was determined by methemoglobin method. Protein sequence was analyzed by (µLC/MS/MS).
Results: A protein of Mr. ~57 kDa was isolated and found to be activated by not only “nitro” compounds but also by acetyl salicylic acid, insulin and glucose. The global BLAST of the protein sequence showed a significant alignment of the protein sequence with PDI. This protein trivially called pluri activator stimulated endothelial NOS (PLASENOS). The enzyme was stimulated by the above-mentioned activators in the presence of Ca2+. Lineweaver-Burk plot of this NOS like activities were demonstrated with its specific substrate l-arginine as Vmax = 5(nmol NO/mg of protein/hr) and Km≈ 0.5µM by the above activators. The enzyme activity was inhibited by the l-NAME, the specific inhibitor of NOS.
Conclusion: The organic nitro compounds, acetyl salicylic acid, insulin and glucose were found to activate PLASENOS in the arterial endothelial cells for a continuous supply of NO to control the chest pain in acute coronary syndrome.
Keywords: Nitro compounds, insulin, nitric oxide, glucose, pain, PLASENOS.
Graphical Abstract
Protein & Peptide Letters
Title:Expression of a Nitric Oxide Synthesizing Protein in Arterial Endothelial Cells in Response to Different Anti-Anginal Agents Used in Acute Coronary Syndromes
Volume: 24 Issue: 11
Author(s): Sarbashri Bank, Pradipta Jana, GV Girish, Asru K Sinha and Smarajit Maiti*
Affiliation:
- Cell & Molecular Therapeutic lab, Department of Biochemistry, Vidyasagar University, Midnapur-721102,India
Keywords: Nitro compounds, insulin, nitric oxide, glucose, pain, PLASENOS.
Abstract: Background: Organic “nitro” compounds such as nitroglycerine, isosorbide dinitrate are useful in the control of chest pain in acute coronary syndrome. But the mechanism of it in pain regulation remains speculative. Here, increase of NO production was investigated by the possible regulation of constitutive nitric oxide synthase (cNOS) function from goat arterial endothelial cells. This protein was purified and sequence wise characterized as protein disulfide isomerase (PDI) in response to different nitro compounds.
Method: The NO generating protein was isolated from arterial endothelial cells and prepared to homogeneity. NO was determined by methemoglobin method. Protein sequence was analyzed by (µLC/MS/MS).
Results: A protein of Mr. ~57 kDa was isolated and found to be activated by not only “nitro” compounds but also by acetyl salicylic acid, insulin and glucose. The global BLAST of the protein sequence showed a significant alignment of the protein sequence with PDI. This protein trivially called pluri activator stimulated endothelial NOS (PLASENOS). The enzyme was stimulated by the above-mentioned activators in the presence of Ca2+. Lineweaver-Burk plot of this NOS like activities were demonstrated with its specific substrate l-arginine as Vmax = 5(nmol NO/mg of protein/hr) and Km≈ 0.5µM by the above activators. The enzyme activity was inhibited by the l-NAME, the specific inhibitor of NOS.
Conclusion: The organic nitro compounds, acetyl salicylic acid, insulin and glucose were found to activate PLASENOS in the arterial endothelial cells for a continuous supply of NO to control the chest pain in acute coronary syndrome.
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Bank Sarbashri , Jana Pradipta, Girish GV, Sinha K Asru and Maiti Smarajit*, Expression of a Nitric Oxide Synthesizing Protein in Arterial Endothelial Cells in Response to Different Anti-Anginal Agents Used in Acute Coronary Syndromes, Protein & Peptide Letters 2017; 24 (11) . https://dx.doi.org/10.2174/0929866524666170911164801
DOI https://dx.doi.org/10.2174/0929866524666170911164801 |
Print ISSN 0929-8665 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5305 |
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